Detecting adenosine triphosphatase 6 point mutations that may be associated with Plasmodium falciparum resistance to artemisinin: prevalence at baseline, before policy change in Uganda

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Fältnamn	Indikatorer	Metadata
000		03224naa a2200397 4500
001		oai:DiVA.org:uu-169794
003		SwePub
008		120306s2011 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1697942 URI
040		a (SwePub)uu
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Kamugisha, Erasmus4 aut
245	1 0	a Detecting adenosine triphosphatase 6 point mutations that may be associated with Plasmodium falciparum resistance to artemisinin :b prevalence at baseline, before policy change in Uganda
264	1	c 2011
338		a electronic2 rdacarrier
520		a The artemisinin based combination therapy (ACT) of artemether and lumefantrine (Co-artem) has recently replaced chloroquine and fansidar as the first line treatment policy drug in Uganda. It is necessary to develop practical procedures to monitor the likely emergence and spread of artemisinin resistant P. falciparum strains. We have analyzed the genotypes of PfATP6 in parasites from 300 stored filter paper samples from malaria patients who were diagnosed and treated in the years 1999 to 2004 at three field sites in Uganda. This is a period just prior to introduction of Co-artem. In order to develop a simple molecular procedure for mutation detection, regions of PfATP6 encoding protein domains important in artemisinin binding was amplified by nested PCR. Three DNA products, which together contain most of the coding region of amino acids located within the putative active site of pfATP6 were readily amplified. The amplified DNA was digested by restriction enzymes and the fragments sized by agarose gel electrophoresis. For the important codons 260, 263 and 769, methods using engineered restriction sites were employed. We did not find mutations at codons for the key residues Lys 260, Leu263, Gln266, Ser769 and Asn1039. Nucleotide sequencing of pfATPase6 gene DNA from at least 15 clinical isolates confirmed the above findings and suggested that mutations at these amino acid residues have not emerged in our study sites.
653		a PfATP5
653		a artemisinin
653		a resistance
653		a SERCA
653		a Plasmodium falciparum
653		a Uganda
700	1	a Sendagire, Hakim4 aut
700	1	a KadduMukasa, Mark4 aut
700	1	a Enweji, Nizaru Uppsala universitet,Institutionen för medicinsk biokemi och mikrobiologi4 aut0 (Swepub:uu)nizen916
700	1	a Gheysari, Fathemeu Uppsala universitet,Institutionen för medicinsk biokemi och mikrobiologi4 aut
700	1	a Swedberg, Göteu Uppsala universitet,Institutionen för medicinsk biokemi och mikrobiologi4 aut0 (Swepub:uu)goteswed
700	1	a Kironde, Fred4 aut
710	2	a Uppsala universitetb Institutionen för medicinsk biokemi och mikrobiologi4 org
773	0	t Tanzania Journal of Health Researchg 13:1, s. 50-60q 13:1<50-60x 1821-6404
856	4	u http://www.bioline.org.br/abstract?id=th11007&lang=en
856	4	u https://uu.diva-portal.org/smash/get/diva2:507709/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-169794

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Av författaren/redakt...: Kamugisha, Erasm ...; Sendagire, Hakim; KadduMukasa, Mar ...; Enweji, Nizar; Gheysari, Fathem ...; Swedberg, Göte; visa fler...; Kironde, Fred; visa färre...

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Av lärosätet: Uppsala universitet

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